Diabetic foot ulcers continue to burden the US healthcare system and patients with an estimated annual cost of $30 billion and amputation rates of 100,000. Unfortunately, the exact etiology of the problem remains to be resolved. Developing effective footwear and intervention strategies to prevent diabetic amputations requires a comprehensive understanding of the ulceration pathway. Diabetic foot lesions are known to have a biomechanical pathology that involves mechanical stresses acting under the foot. Foot pressure alone is not a good predictor of ulcers, since ulcers might occur at pressure levels that are not considered harmful. Results regarding the pathological effects of plantar shear are not yet conclusive. Preventive footwear, designed to only relieve peak pressures are just meagerly effective in preventing ulceration which can be attributed to the fact that exact pathology of ulcers has unresolved issues. An alternative theory regarding ulceration states that peripheral neuropathy leads to unvarying patterns of plantar loading in diabetic patients, which may consequently result in tissue tenderness and breakdown. Healthy individuals were shown to shift their loading patterns, which prevents tissue tenderness and pain at the regional scale. Due to neuropathy, certain regions of the diabetic foot are thought to experience repetitive stresses that are not relieved. Prolonged repetition might result in failure of the tissue even wit lower, yet unrelieved, mechanical stresses. Higher plantar temperatures are also associated with ulcer development. Treadmill walking for 10 minutes leads to a substantial temperature increase in healthy feet. This increase can possibly be higher in diabetic patients due to higher plantar stresses, which has not been yet studied. Walking-induced plantar temperature increase has been used as a predictor of triaxial plantar loading. However this hypothesis has not been validated. In order to test these hypotheses, we aim at; (1) investigating the variability of triaxal plantar loading in diabetic neuropathic patients, (2) comparing the variability of triaxial plantar loading between the neuropathic group and two control groups, and (3) quantifying stress-induced plantar temperature increase and correlating this with plantar stresses. For specific Aim 1, plantar pressure and shear profiles of diabetic patients will be collected at different time points during a day. If unvarying stress profiles are confirmed in diabetic patients, this factor wll be considered as a risk for ulceration. For specific aim 2, we will use the same methodology to assess the variability of triaxial plantar loading in diabetic neuropathic and control subjects. Variability across sessions will be compared between the three subject groups. Significantly different (lower) variability in neuropathic subjects will indicate the clinical importance of this factor in ulceration. For specific aim 3, we will quantify plantar temperature increases due to prolonged walking in subject groups. This temperature increase will be correlated against triaxial plantar stress magnitudes. Based on information acquired in this study, more effective preventive devices and strategies may be developed to reduce ulcer incidences.